ArticleThe Journal of experimental medicine2010
Elevated expression of TDP-43 in the forebrain of mice is sufficient to cause neurological and pathological phenotypes mimicking FTLD-U.
Article in The Journal of experimental medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 129 papers.
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Who cites it
129 citing papers in PubMed, 238 citations in OpenAlex.
- Human TDP-43 expression worsens FTD-related phenotypes in progranulin-insufficient mice.Neurobiology of disease · 2026Article
- Selective Brain-Penetrant TTBK1 Inhibitors Modulate TDP-43 Pathology and Rescue Cognitive Deficits in a Mouse Model of TDP-43 Proteinopathy.Journal of medicinal chemistry · 2026Article
- Defining the Intestinal eCBome and Oxylipin Signaling Systems in a TDP-43 Mouse Model of Frontotemporal Dementia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Astrocytes expressing mutant hnRNPA1 induce non-cell-autonomous motor neuron death.Brain research bulletin · 2025Article
- Challenges of modelling TDP-43 pathology in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Deep learning-driven MRI for accurate brain volumetry in murine models of neurodegenerative diseases.Frontiers in neuroscience · 2025Article
- Beneficial Effect of Dimethyl Fumarate Drug Repositioning in a Mouse Model of TDP-43-Dependent Frontotemporal Dementia.Antioxidants (Basel, Switzerland) · 2024Article
- Elevated nuclear TDP-43 induces constitutive exon skipping.Molecular neurodegeneration · 2024Article
- Increase in hnRNPA1 Expression Suffices to Kill Motor Neurons in Transgenic Rats.International journal of molecular sciences · 2023Article
- Article
- Preclinical investigation in FAAH inhibition as a neuroprotective therapy for frontotemporal dementia using TDP-43 transgenic male mice.Journal of neuroinflammation · 2023Article
- Transthyretin attenuates TDP-43 proteinopathy by autophagy activation via ATF4 in FTLD-TDP.Brain : a journal of neurology · 2023Article
- Synaptic Dysfunction and Plasticity in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- Codon-optimized TDP-43 mediates neurodegeneration in aFrontiers in genetics · 2023Article
- Neural circuit and synaptic dysfunctions in ALS-FTD pathology.Frontiers in neural circuits · 2023Review
- New Statement about NRF2 in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.Biomolecules · 2022Article
- Short-Term Cortical Electrical Stimulation during the Acute Stage of Traumatic Brain Injury Improves Functional Recovery.Biomedicines · 2022Article
- Estrogen Enhances Dendrite Spine Function and Recovers Deficits in Neuroplasticity in the prpTDP-43Molecular neurobiology · 2022Article
- Review
- Dysregulation of Translation in TDP-43 Proteinopathies: Deficits in the RNA Supply Chain and Local Protein Production.Frontiers in neuroscience · 2022Review
69 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TDP-43 is a multifunctional DNA/RNA-binding factor that has been implicated in the regulation of neuronal plasticity. TDP-43 has also been identified as the major constituent of the neuronal cytoplasmic inclusions (NCIs) that are characteristic of a range of neurodegenerative diseases, including the frontotemporal lobar degeneration with ubiquitin(+) inclusions (FTLD-U) and amyotrophic lateral sclerosis (ALS). We have generated a FTLD-U mouse model (CaMKII-TDP-43 Tg) in which TDP-43 is transgenically overexpressed in the forebrain resulting in phenotypic characteristics mimicking those of FTLD-U. In particular, the transgenic (Tg) mice exhibit impaired learning/memory, progressive motor dysfunction, and hippocampal atrophy. The cognitive and motor impairments are accompanied by reduced levels of the neuronal regulators phospho-extracellular signal-regulated kinase and phosphorylated cAMP response element-binding protein and increased levels of gliosis in the brains of the Tg mice. Moreover, cells with TDP-43(+), ubiquitin(+) NCIs and TDP-43-deleted nuclei appear in the Tg mouse brains in an age-dependent manner. Our data provide direct evidence that increased levels of TDP-43 protein in the forebrain is sufficient to lead to the formation of TDP-43(+), ubiquitin(+) NCIs and neurodegeneration. This FTLD-U mouse model should be valuable for the mechanistic analysis of the role of TDP-43 in the pathogenesis of FTLD-U and for the design of effective therapeutic approaches of the disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.